Cell death and the glutathione S-transferase alpha overexpression induced by the natural anticarcinogen sulforaphane in Caco2 cells follow independent pathways. - INRAE - Institut national de recherche pour l’agriculture, l’alimentation et l’environnement Accéder directement au contenu
Article Dans Une Revue NAFAS Science Année : 2005

Cell death and the glutathione S-transferase alpha overexpression induced by the natural anticarcinogen sulforaphane in Caco2 cells follow independent pathways.

Patrick Rouimi
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Thierry Fricaux
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Nicole Gasc
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Jacques Tulliez
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Laurence Gamet-Payrastre

Résumé

Consensus has been building that diets rich in fruits and vegetables are associated with lower risks of developing various type of cancer. Increasing evidence suggest a link between prevention of carcinogenesis and natural isothiocyanate intakes provided by a normal consumption of cruciferous vegetables. Isothiocyanates occur in the vegetal as biologically inactive thioglucosides, which are processed by plant or intestinal microflora myrosinases, and have been described as effective inhibitors of chemically induced carcinogenesis in animal models. Indeed, sulforaphane, an isothiocyanate from broccoli, was shown to protect carcinogen-treated rats from tumorigenesis. Little is known about the mechanism by which sulforaphane operates, except that it involves -at least in part- phase I enzymes inhibition, phase II enzymes induction, cell cycle arrest and/or apoptosis. Therefore, we investigate possible intracellular targets of SFN using human colon carcinoma cell lines. In an earlier study, we showed that sulforaphane-induced apoptosis and cell cycle arrest at the G2/M phase in HT29 cells. We now investigate MAP kinase modulation, glutathione S-transferase expression and the tyrosine kinase phosphorylation status in the similar cell model, Caco2. We also compared some parameters from the well-described cell differentiation induced by sodium butyrate to sulforaphane effects. Our results show that sulforaphane induces cell death through ERK1/2 and transient P38 activation. Involvement of JNK is less clear. On an other hand, the strong induction of class alpha GSTs observed as well in confluent/differentiated untreated cells as in exponentially-growing Caco2 cells exposed to sulforaphane, appears independent of the MAP kinase pathway. In addition, sulforaphane properties do not seem to be related with a marked histone hyperacetylation in this cell model.
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hal-02676027 , version 1 (31-05-2020)

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  • HAL Id : hal-02676027 , version 1
  • PRODINRA : 483261

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Patrick Rouimi, Thierry Fricaux, Nicole Gasc, Nathalie Druesne, Jacques Tulliez, et al.. Cell death and the glutathione S-transferase alpha overexpression induced by the natural anticarcinogen sulforaphane in Caco2 cells follow independent pathways.. NAFAS Science, 2005, 3, pp.97-106. ⟨hal-02676027⟩
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